Blood Gas Analysis PDF

BLOOD GAS ANALYSIS MIMV 3rd year – 1st semester 15 September 2024 Ricardo Felisberto, DVM, Dipl. ECVAA, MRCVS  pH Sorensen proposed the definition of pH: The logarithm of the inverse of the Hydro...

BLOOD GAS ANALYSIS MIMV 3rd year – 1st semester 15 September 2024 Ricardo Felisberto, DVM, Dipl. ECVAA, MRCVS  pH Sorensen proposed the definition of pH: The logarithm of the inverse of the Hydrogen ions concentration (if H+ concentration increases = pH decreases) 1 pH = Log10[𝐻+] Arrhenius definition of acid: Substance that yields hydrogen ions in aqueous solution Scale 0 – 14 (< 7.0 = acid; > 7.0 = alkaline) pH Buffer: Substance that acts to normalize a pH disturbance Carbonic acid (H2CO3) is an example of pH buffer (weak acid) CO2 + H2O → H2CO3 → HCO3- + H+ The reactions occur bidirectionally, to bind CO2 + H2O carbonic anhydrase enzyme is required (mostly locate intracellularly) Le Chateliers principle: if one side of the equation increases, then this pushes the reaction to the opposite side, for example: If there is an increase in H+ it pushes the reaction to the left If there is an increase in CO2 it pushes the reaction to the right  pH Henderson-Hasselbalch equation: if 𝐻𝐶𝑂3− pH = pKa + log10 α 𝑥 𝑃𝑎𝐶𝑂2 The pKa is of the carbonic acid (6.1); α is a solubility coefficient of CO2 (0.03 mmol/L/mmHg). According to this equation, there must be a stable ratio of CO2 and HCO3- to maintain the pH stable (usually, 1 of HCO3- to 20 of CO2). Therefore, if one increases the other one must increase too, to maintain pH. Why is it important to maintain pH stable?: To maintain optimal enzymatic activity (7.35 – 7.45); incompatible with life (< 6.8; > 7.6)  pH In the blood: If pH is < 7.35 = Acidaemia If pH is > 7.45 = Alkalemia The causes for these derangements are: Acidosis or Alkalosis (there are the processes that may or may not lead to acidaemia and alkalemia, respectively) Derangements: Respiratory acidosis: hypoventilation; pulmonary or pleural disease; intercostal or diaphragmatic muscles paralysis; respiratory obstruction. Respiratory alkalosis: hyperventilation (secondary to anaemia, hypoxemia); increased settings on positive pressure ventilation; fear; excitement; pain; hyperthermia. Metabolic acidosis: ketoacidosis (diabetes mellitus); lactic acidosis; diarrhoea (bicarbonate loss); kidney failure (less acid excretion or bicarbonate loss); saliva loss of bicarbonate. Metabolic alkalosis: iatrogenic bicarbonate administration; vomiting (loss of acid stomach content); abomasal acid sequestration.  pH REGULATION There are 3 main systems: Chemical buffers Respiratory system Kidneys Chemical buffers in extracellular (ECF) and intracellular fluids (ICF) (act in seconds): ECF buffers: act immediately ICF buffers: act after Examples: Bicarbonate; Phosphate; Ammonia/Ammonium; Proteins (ECF = albumin +++; ICF = haemoglobin +++); Transcellular H+/K+ ion exchanger These buffers will bind or dissociate from the H+ according to the primary derangement. Respiratory system (act in minutes to hours): Increasing the alveolar ventilation will drop the PaCO2 in the presence of a metabolic acidosis Kidneys (act in hours to days): Excrete / reabsorb acids or bases Liver and GI tract produce glutamine which is metabolised by the renal proximal tubular cells to bicarbonate and ammonia (bicarbonate is regained; Ammonia and phosphate are excreted)  pH REGULATION How do these buffer systems work together?: The chemical buffers act immediately: In blood the most important buffer system is the bicarbonate; but also, phosphate and proteins. Carbonic anhydrase enzyme catalyses the reaction CO2 + H2O → H2CO3 (its present mostly intracellularly, as the intracellular pH is lower than 7.4, or closer to the carbonic acid pKa, thus this reaction occurs mostly intracellularly). The bicarbonate buffer is also relevant in the ECF due to its high abundance. The respiratory system starts working after if the chemical buffers are insufficient to correct the derangement: pH may not normalise even if the CO2 has changed. There is a limit of how much the CO2 can change, because too high CO2 leads to excessive cerebral vasodilation and stimulation of the respiratory centre; and too low CO2 causes cerebral vasoconstriction (syncope) and inhibition of the respiratory centre. Kidneys: Will be involved if the first 2 are not enough to correct the derangement. Bicarbonate re-absorption; Acid excretion, or vice-versa depending on the primary derangement.  OXYGENATION AND VENTILATION e evaluate how well a person is breathing (ventilating) by measuring the partial pressure of carbon dioxide (CO₂) in their arterial blood Oxygenation assessed by the partial pressure of oxygen (PaO2) Hypoxaemia: Refer to amount of O2 in blood and assessed by partial pressure of O2 in arterial blood Mild: 60 – 80 mmHg PaO2 Normal PaO₂: Usually between 80-100 mmHg. Hypoxemia (low oxygen levels in the blood): Severe: < 60 mmHg PaO2 Mild Hypoxemia: PaO₂ of 60-80 mmHg. Hyperoxaemia: Severe Hypoxemia: PaO₂ of less than 60 mmHg. Hyperoxemia (excessively high oxygen levels): > 100 mmHg PaO2 PaO₂ greater than 100 mmHg. Ventilation assessed by the partial pressure of carbon dioxide (PaCO2) Hypoventilation: > 45 mmHg PaCO2 Hyperventilation: < 35 mmHg PaCO2 Ventilation: body’s ability to expel CO2 (which is measured by PaCO2 in arterial blood Normal PaCO₂: Typically between 35-45 mmHg. Hypoventilation: PaCO₂ greater than 45 mmHg (inadequate ventilation, causing CO₂ retention and respiratory acidosis). Hyperventilation: PaCO₂ less than 35 mmHg (excessive ventilation, causing CO₂ elimination and respiratory alkalosis)  how well the lungs are oxygenating blood and pinpoint the cause of hypoxemia (low blood oxygen level) INDICES OF OXYGENATION PaO2: partial pressure of O2 in arterial blood vs PAO2: partial pressure of O2 in alveolar air (lung) normal= +0.85 if less severe venous admixture mean deoxygenated venous blood is mixing with oxygenated arterial blood reducing oxygen delivery PaO2 : PAO2 ratio: if < 0.85 = severe venous admixture PaO2 : PaCO2: if > 140 mmHg at room air = lungs oxygenate blood normally; if < 120 mmHg = venous admixture. PaO2 : FiO2 ratio: Normal (450 – 330 mmHg); Acute lung injury (< 300 mmHg); Acute respiratory distress syndrome (< 200 mmHg). P(A-a)O2 Difference: normal should be 60 – 70 mmHg = intervene with positive pressure ventilation. < 20 mmHg should be avoided due to high cerebral vascular resistance and brain ischaemia. 45 – 60 mmHg: Increases Sympathetic nervous system and increase in catecholamines; plus, it decreases affinity of haemoglobin to oxygen (facilitates oxygen delivery to the tissues) – advantageous. Causes cerebral vasodilation, which increases the cerebral blood flow and intracranial pressure – disadvantageous. When PaCO2 ↑ = the reaction of the carbonic acid is pushed in the direction of the production of H+ and bicarbonate. The increase of H+ concentration decreases the pH. Although bicarbonate is also produced, the pH decreases due to the increase in H+ concentration.  INTERPRETATION OF ARTERIAL BLOOD GAS Bicarbonate: It should increase if the PaCO2 increases (its change should be in the same direction as for the PaCO2) → if not, mixed disorder The ratio of PaCO2:Bicarbonate should be maintained of 1:20 It can be decreased due to loss or consumption, anion gap can be used to determine which one is more likely in the face of metabolic acidosis.  INTERPRETATION OF ARTERIAL BLOOD GAS Base excess: Actual Base Excess: Dose of acid or alkali (mmol) required to return the blood pH to 7.4 (1L of blood) → represents all buffering systems (bicarbonate, phosphate, haemoglobin, plasma proteins) Standard Base Excess: Dose of acid or alkali (mmol) required to return the blood pH to 7.4 (1L of anaemic blood) → represents the buffering systems except the haemoglobin, because it considers only the buffering systems of the ECF. Normal: -4 to 4 mmol/L It represents the buffering ability of all chemical buffers present. If there is a decreased buffering capacity, we should have a low or negative base excess; if there is an increased buffering capacity, we should have a high or positive base excess. Metabolic Acidosis: negative base excess Metabolic Alkalosis: positive base excess  INTERPRETATION OF ARTERIAL BLOOD GAS Administer bicarbonate only if these three topics are together: If the BE is more negative than – 7 mmol/L If the pH is lower than 7.1 If the bicarbonate is low (due to loss of bicarbonate; if the acidaemia is due to acids accumulation, bicarbonate may not be the best option – e.g., lactic acidosis due to hypovolaemia; correct the hypovolaemia) mmol bicarbonate required = BE x 0.3 x kg → give first half as slow bolus; wait 20 minutes, re-evaluate blood gas analysis and administer or not the second half. Problems with bicarbonate administration: Haemodilution: ↓ PCV (care if animal already anaemic); ↓ total proteins; ↓ platelets; ↓ clotting factors; hypochloraemia Hypernatremia: bicarbonate is administered in the form of sodium bicarbonate Volume expansion: bicarbonate is hyperosmolar, which makes extravascular fluid movement into the intravascular space. Hypercapnia: the load of bicarbonate pushes the reactions to produce CO2, particularly intracellularly (where there is more carbonic anhydrase); this can worsen the acidotic process; thus ventilation should be frequently checked when administering bicarbonate. Alkalosis Ionised hypocalcaemia: increased pH will increase the binding of ionised calcium to albumin. Hypokalaemia: increased pH stimulates the movement of H+ from intracellular to extracellular with exchange with potassium in the inverse way (H+/K+ exchanger)  INTERPRETATION OF ARTERIAL BLOOD GAS Anion gap (AG): Difference between measured cations and measured anions: Na+ + K+ + unmeasured cations = Cl- + HCO3- + unmeasured anions AG = Na+ + K+ = Cl- + HCO3- Not all anions can be measured routinely (acid lactic; acetoacetate; β-hydroxybutyrate; phosphate; sulphates; proteins): This leads to a difference between the cations and anions (cations more than anions) Normal: Dogs: 12 – 25 mmol/L Cats: 13 – 27 mmol/L If there is a metabolic acidosis; the AG will help to understand if the cause is due to: HCO3- Loss: If bicarbonate is lost due to the disease process, to maintain electroneutrality, the Chloride ion will increase; this leads to the maintenance of normal AG (hyperchloraemic metabolic acidosis). Caused by: renal loss; GI loss; NaCl administration; hypoadrenocorticism. Accumulation of unmeasured anions: Increase of these anions, leads to bicarbonate consumption, but without change in chloride ion (because the unmeasured anions are already high), this leads to a high AG (normochloraemic metabolic acidosis) Caused by: DUEL, Diabetic ketoacidosis; Uraemia; Ethylene glycol intoxication; Lactic acidosis.  COMPENSATORY MECHANISMS For acute respiratory acidosis: For each ↑ of 10 mmHg PaCO2 = ↑ HCO3- by 1.5 mmol/L For chronic respiratory acidosis: For each ↑ of 10 mmHg PaCO2 = ↑ HCO3- by 3.5 mmol/L For acute respiratory alkalosis: For each ↓ of 10 mmHg PaCO2 = ↓ HCO3- by 2.5 mmol/L For chronic respiratory alkalosis: For each ↓ of 10 mmHg PaCO2 = ↓ HCO3- by 5.5 mmol/L For metabolic acidosis: For each ↓ of 1 mmol HCO3- = ↓ PaCO2 by 0.7 mmHg For metabolic alkalosis: For each ↑ of 1 mmol HCO3- = ↑ PaCO2 by 0.7 mmHg For each ↑ of 10 mmHg PaCO2 = ↓ 0.08 units of pH  CLINICAL CASE EXAMPLE Dog, 12-year-old, labrador with 3 weeks history of diarrhoea. Arterial blood sample at room air (FiO 2 21%) 1. Acidaemia: Variable Results Reference range a) Metabolic acidosis. b) Respiratory acidosis. pH 7.261 7.35 – 7.45 c) Both. PCO2 (mmHg) 26.9 27.8 – 47.2 2. Hypocapnia: a) Hyperventilation. PO2 (mmHg) 98 85 – 100 b) Respiratory alkalosis as compensation to metabolic BEecf (mmol/L) -6 -5 - +5 acidosis. 3. Bicarbonate: HCO3- (mmol/L) 14.6 18.3 – 26.4 a) Low (loss or consumption) SO2 (%) 100 >90 4. Base excess: a) Low (metabolic acidosis process) Na+ (mmol/L) 148 139 – 150 5. Oxygenation: K+ (mmol/L) 4.2 3.4 – 4.7 a) Normal 6. Anion Gap: Cl- (mmol/L) 124 110 – 120 a) Normal; hyperchloraemic metabolic acidosis (due AG (mmol/L) 13.6 12 - 25 to loss of bicarbonate)